The recent explo­sion of inter­est in “epi­ge­net­ics” — a term lit­er­ally mean­ing “around the gene,” and refer­ring to any­thing that changes a gene’s effect with­out chang­ing the actual DNA sequence — has tended to focus on the long game of gene-​environment inter­ac­tions: how famine among expec­tant moth­ers in the Nether­lands dur­ing World War II, for instance, affected gene expres­sion and behav­ior in their chil­dren; or how mother rats, by lick­ing and groom­ing their pups more or less assid­u­ously, can alter the wrap­pings around their offspring’s DNA in ways that influ­ence how anx­ious the pups will be for the rest of their lives. The idea that expe­ri­ence can echo in our genes across gen­er­a­tions is cer­tainly a pow­er­ful one. But to focus only on these nar­row, long-​reaching effects is to miss much of the action where epi­ge­netic influ­ence and gene activ­ity is con­cerned. This fresh work by Robin­son, Fer­nald, Clay­ton, and oth­ers — encom­pass­ing stud­ies of mul­ti­ple organ­isms, from bees and birds to mon­keys and humans — sug­gests some­thing more excit­ing: that our social lives can change our gene expres­sion with a rapid­ity, breadth, and depth pre­vi­ously overlooked.

Why would we have evolved this way? The most prob­a­ble answer is that an organ­ism that responds quickly to fast-​changing social envi­ron­ments will more likely sur­vive them. That organ­ism won’t have to wait around, as it were, for bet­ter genes to evolve on the species level. Immu­nol­o­gists dis­cov­ered some­thing sim­i­lar 25 years ago: Adapt­ing to new pathogens the old-​fashioned way — wait­ing for nat­ural selec­tion to favor genes that cre­ate resis­tance to spe­cific pathogens — would hap­pen too slowly to counter the rapidly chang­ing pathogen envi­ron­ment. Instead, the immune sys­tem uses net­works of genes that can respond quickly and flex­i­bly to new threats.

We appear to respond in the same way to our social envi­ron­ment. Faced with an unpre­dictable, com­plex, ever-​changing pop­u­la­tion to whom we must respond suc­cess­fully, our genes behave accord­ingly — as if a fast, fluid response is a mat­ter of life or death.

Schiz­o­phre­nia and Genet­ics— does crit­i­cal thought stop here? by Mary Boyle at a con­fer­ence enti­tled “From Gal­ton to the Human Genome Project: A crit­i­cal appraisal of genetic the­o­ries in psy­chol­ogy and psy­chi­a­try”, 2004

Psy­chi­a­trists and neu­ro­sci­en­tists around the world recently have begun sound­ing the alarm that the field is in cri­sis. Drug devel­op­ment for com­plex psy­chi­atric ill­nesses is mis­guided, they argue, stuck churn­ing out slight vari­a­tions on ther­a­peu­tic themes that didn’t work all that well to begin with. Faulty assump­tions, ani­mal mod­els that don’t look any­thing like human dis­eases, hazy diag­noses and a lack of knowl­edge about how the brain works have all thwarted the search for bet­ter drugs.

But then it goes on to say that they need a bet­ter under­stand­ing of genes and mol­e­cules in order to under­stand why “1 out of 4 peo­ple are men­tally ill” and why so many peo­ple suf­fer from men­tal afflic­tion, in their opin­ion. With 1 out of 4 as an esti­mate, how could envi­ron­ment be an issue? How could any of the diag­noses be bunk? Yes. Snark.

Schiz­o­phre­nia researcher Tim­o­thy Crow wrote in 2008 that mol­e­c­u­lar genetic researchers inves­ti­gat­ing psy­chotic dis­or­ders such as schiz­o­phre­nia had pre­vi­ously thought that “suc­cess was inevitable-​one would ‘drain the pond dry’ and there would be the genes!” But as Crow con­cluded, “The pond is empty.” Four years later the psy­chi­atric dis­or­der and psy­cho­log­i­cal trait “gene ponds” appear to have been com­pletely drained, and there are few if any genes to be found. Twenty years ago, how­ever, lead­ing behav­ioral geneti­cists had high expec­ta­tions that mol­e­c­u­lar genetic research would soon “rev­o­lu­tion­ize” the behav­ioral sciences.

wiley­witch sez: Though it is widely con­sid­ered to be axiomatic that men­tal ill­ness is genet­i­cally deter­mined, upon analy­sis most of the research show­ing a con­cor­dance is, at best, ques­tion­able, and at times fraudulent.

Today, it is widely acknowl­edged by pro­po­nents of the genetic posi­tion that fam­ily stud­ies are con­founded by envi­ron­men­tal fac­tors, since fam­ily mem­bers share both com­mon genes and a com­mon envi­ron­ment. As a pair of psy­chi­atric geneti­cists recently put it, fam­ily stud­ies can pro­vide only “the ini­tial hint that a dis­or­der might have a genetic component”

This is what I like to call, “Have I men­tioned that I lived with my mother?” A state­ment that has too often been met with what I call the “ther­a­peu­tic glaze.”

A ques­tion about iden­ti­cal twins sep­a­rated at birth

…let us sup­pose that a 20 year-​old pair of Ger­man reared-​apart male MZ twins, sep­a­rated at birth and brought up in dif­fer­ent parts of the coun­try, had been reunited in 1940. A researcher would prob­a­bly notice sev­eral strik­ing sim­i­lar­i­ties. Both might be wear­ing swastika arm­bands, have short-​cropped hair, give stiff arm salutes and rail against “the ene­mies of the Reich.” The val­ues, beliefs, behav­iors, and even wardrobes of these twins might be remark­ably sim­i­lar, yet the con­clu­sion that these sim­i­lar­i­ties are caused by com­mon genes would be quite erroneous.